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Air pollution has been reported to be associated with increased risks of cognitive impairment and neurodegenerative diseases. Because NO 2  is a typical primary air pollutant and an important contributor to secondary aerosols, NO 2 -induced neuronal functional abnormalities have attracted greater attention, but the available experimental evidence, modulating mechanisms, and targeting medications remain ambiguous. In this study, we exposed C57BL/6J and APP/PS1 mice to dynamic NO 2  inhalation and found for the first time that NO 2  inhalation caused deterioration of spatial learning and memory, aggravated amyloid β 42  (Aβ 42 ) accumulation, and promoted pathological abnormalities and cognitive defects related to Alzheimer’s disease (AD). The microarray and bioinformation data showed that the cyclooxygenase-2 (COX-2)-mediated arachidonic acid (AA) metabolism of prostaglandin E 2  (PGE 2 ) played a key role in modulating this aggravation. Furthermore, increasing endocannabinoid 2-arachidonoylglycerol (2-AG) by inhibiting monoacylglycerol lipase (MAGL) prevented PGE 2  production, neuroinflammation-associated Aβ 42  accumulation, and neurodegeneration, indicating a therapeutic target for relieving cognitive impairment caused by NO 2  exposure.

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NO2 inhalation promotes Alzheimer’s disease-like progression: cyclooxygenase-2-derived prostaglandin E2 modulation and monoacylglycerol lipase inhibition-targeted medication